Cases reported "Glioblastoma"

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1/754. Severe ocular and orbital toxicity after intracarotid etoposide phosphate and carboplatin therapy.

    PURPOSE: To report severe ocular and orbital toxicity after administration of intracarotid etoposide phosphate and carboplatin. METHOD: Case report. RESULTS: A 52-year-old man with glioblastoma multiforme underwent left intracarotid administration of eto poside phosphate and carboplatin inferior to the ophthalmic artery. Within 7 hours, a nonpupillary block angle-closure glaucoma developed secondary to uveal effusion in the ipsilateral eye, which was relieved by cycloplegia. Four days later, severe orbital inflammation resulted in a visual acuity of counting fingers, proptosis, optic neuropathy, and total external ophthalmoplegia in the eye. The patient's condition improved after a lateral cantholysis and administration of high-dose intravenous corticosteroids. Two weeks later, an anterior uveitis occurred in the left eye, which responded to topical corticosteroids. During a 2-month period, the patient recovered to a visual acuity of 20/70, near normal motility, and normal intraocular pressure, and the ocular and orbital inflammation resolved. Preexisting ipsilateral chemotherapy-induced maculopathy became more pronounced. CONCLUSION: Ocular and orbital toxicity after intracarotid etoposide phosphate and carboplatin therapy is infrequently reported. ( info)

2/754. Secondary glioblastoma remarkably reduced by steroid administration after anaplastic transformation from gliomatosis cerebri--case report.

    A 45-year-old female presented with gliomatosis cerebri manifesting as hemiballismus-like involuntary movement in the arm, motor weakness in the leg, and hypesthesia in her left side. Computed tomography showed only diffuse swelling of the right cerebral hemisphere, but T2-weighted magnetic resonance imaging revealed a diffuse lesion spreading from the right thalamus to the temporal, parietal, and occipital lobes on the same side. No abnormal enhancement was recognized. cerebral angiography showed no specific finding. A right occipital lobectomy was performed to confirm the diagnosis of gliomatosis cerebri. Anaplastic transformation was recognized 5 months later. The disease did not resolve with radiation or interferon administration, but steroid therapy achieved remarkably effective tumor regression. The patient died due to pneumonia. autopsy showed the features of diffuse glioblastoma. Steroid therapy may be an effective treatment for gliomatosis cerebri before the terminal stage. ( info)

3/754. Endobronchial metastasis of glioblastoma multiforme diagnosed by fiberoptic bronchoscopic biopsy.

    We report a case of extraneural metastasis of an intracranial glioblastoma multiforme (GBM) to the left upper lung, in which fiberoptic bronchoscopy played a key role in the diagnosis. The patient, a 20-year-old woman, presented with dry cough and hoarseness 2 years after total excision of the brain tumor and postoperative radiotherapy. Tissue samples obtained during fiberoptic bronchoscopic biopsy had the same morphologic appearance as the primary intracranial tumor, which was consistent with GBM. In cases of pulmonary metastasis of GBM, antemortem diagnosis is rare. Our experience from this case suggests that fiberoptic bronchoscopy may be a valuable diagnostic tool for metastatic GBM. ( info)

4/754. Graphic analysis of microscopic tumor cell infiltration, proliferative potential, and vascular endothelial growth factor expression in an autopsy brain with glioblastoma.

    BACKGROUND: growth of brain tumors requires tumor-cell attachment to adjacent structures, degradation of surrounding matrixes, migration of tumor cells, proliferation of vasculature, and tumor cell proliferation. Comparison of the findings on neuroimaging, degrees and patterns of tumor invasion, regional tumor cell viability detected by Ki-67 immunohistochemistry, and regional vascular endothelial growth factor (VEGF) expression in whole-brain specimen of glioblastoma therefore is of great interest, and will facilitate study of the host reaction against the glioblastoma. methods: We graphically analyzed microscopic tumor-cell infiltration, regional differences in Ki-67 labeling indices (LI), and immunohistochemical expression of VEGF in an autopsy brain with glioblastoma. RESULTS: glioblastoma cells infiltrated the brain far beyond the gross limits of the tumor and the areas with high signal intensity on T2-weighted magnetic resonance images. A wide range of histologic malignancy was apparent from hematoxylin-eosin staining and the Ki-67 labeling indices. VEGF was highly expressed in normal astrocytes located outside the tumor. CONCLUSION: Graphic analysis of histologic and immunohistochemical patterns is a useful method of investigating the mechanisms of glioma growth, tumor cell infiltration in the brain, and the host reaction of the brain against neoplasms. ( info)

5/754. Isolated oculomotor nerve palsy: an unusual presentation of glioblastoma multiforme. Case report and review of the literature.

    The authors present a case of a very unusual clinical presentation of an intra-axial supratentorial glioblastoma multiforme (GBM) in a 63 year old diabetic female patient presenting with a three week history of left progressive complete oculomotor nerve palsy. CT scan and magnetic resonance imaging of the head revealed a left intra-axial mesial temporal glioblastoma multiforme. Operative resection and microscopic examination of a tissue specimen confirmed the diagnosis. The nature of the tumor, the pattern of spread and the postulated mechanisms of such a presentation are discussed. The authors suggest including the diagnosis of GBM in the differential diagnosis of patients with isolated complete oculomotor nerve palsy at the appropriate age group. ( info)

6/754. The hPMS2 exon 5 mutation and malignant glioma. Case report.

    patients with Turcot syndrome (TS) are predisposed to colon tumors and primary brain tumors, typically glioblastomas or medulloblastomas. The authors describe a patient with TS featuring a known germline mutation of exon 5 of the hPMS2 mismatch repair gene who developed two metachronous glioblastomas, both with distinct oligodendroglial features. Molecular genetic analysis revealed allelic loss of chromosome 19q in the patient's second tumor but no allelic loss of chromosome 1p. Prominent microsatellite instability was also found in this tumor, consistent with a germline mismatch repair defect. Because this patient had an unusual underlying condition and his tumor had a unique histological appearance for TS, it was hypothesized that this genetic defect may predispose to malignant gliomas with oligodendroglial features. The authors therefore evaluated whether sporadic glioblastomas and oligodendrogliomas undergo mutations of this region of the hPMS2 gene. However, single-strand conformation polymorphism analysis of hPMS2 exon 5 failed to reveal mutations in 20 sporadic glioblastomas and 16 sporadic oligodendroglial gliomas. Thus, although it is possible that the germline hPMS2 exon 5 mutation may predispose to glioblastomas with an oligodendroglial component, the same genetic defect is not commonly involved in sporadic oligodendrogliomas or glioblastomas. ( info)

7/754. Decreased BOLD functional MR activation of the motor and sensory cortices adjacent to a glioblastoma multiforme: implications for image-guided neurosurgery.

    A patient with a glioblastoma multiforme and mild sensorimotor deficits had significantly less activation of the motor and sensory cortices on the side with the tumor than on the contralateral side on blood oxygen level-dependent (BOLD) functional MR images. This difference, which may be due to pressure effects or loss of vascular autoregulation, should be considered in preoperative planning in which BOLD functional MR imaging is used to identify eloquent cortices to be avoided during brain tumor surgery. ( info)

8/754. Malignant supratentorial ganglioglioma (ganglion cell-giant cell glioblastoma): a case report and review of the literature.

    BACKGROUND: From both epidemiologic and pathologic viewpoints, gangliogliomas exhibiting components of giant cell glioblastomas are extraordinary neoplasms. We report herein the case of a 6-year-old girl who presented initially with a World Health Organization grade IV anaplastic ganglioglioma (a mixed ganglion cell tumor-giant cell glioblastoma). Despite aggressive management, the patient died of disease in a relatively short period. methods: Formalin-fixed, paraffin-embedded tissue blocks were sectioned at 5 microm for histochemical and immunohistochemical analyses. hematoxylin-eosin-stained sections and immunohistochemically stained sections from the primary and secondary resections were reviewed. Reactivity for glial fibrillary acidic protein, neurofilament protein, synaptophysin, and Ki67 nuclear antigen was evaluated. RESULTS: Histologically, 2 distinct cell populations were noted on both the primary and secondary resections. The primary resection revealed a neoplasm having a predominant glial component consistent with a glioblastoma. Interspersed were dysmorphic ganglion cells supporting a diagnosis of ganglioglioma. The second resection (following therapy) demonstrated a much more prominent dysmorphic ganglion cell component and a subdued glial component. CONCLUSION: Although immunohistochemical analysis clearly distinguished the 2 tumor cell populations, the identification of Nissl substance in neurons proved to be equally helpful. Although other cases of grade III gangliogliomas and rare cases of grade IV gangliogliomas have been reported, the present case is exceptional in that, to our knowledge, it is the only report of a patient who presented initially with a composite grade IV ganglioglioma and who was clinically followed up to the time of death. This case allows direct comparison between the histologic findings in a giant cell glioblastoma and a ganglioglioma and documents the aggressive biologic behavior of this complex neoplasm. ( info)

9/754. Gliomatosis cerebri with secondary glioblastoma formation: report of two cases.

    The clinicopathological features of two cases of gliomatosis cerebri associated with secondary glioblastoma formation are reported. In both cases, glial cells were diffusely distributed in the supra- and infratentorial regions and underlying brain structures were preserved from the onset. In spite of such diffuse distribution of neoplastic glial cells, similar to that observed in low-grade astrocytoma, in both cases the tumor underwent complete remission after radiotherapy. However, the tumor recurred as a localized glioblastoma in both cases, 37 months (case 1) and 7 months (case 2) after the radiotherapy. In both cases, recurrence was accompanied by prominent dissemination of CSF. The recurrent tumors were radiation resistant, and the patients' conditions deteriorated rapidly after recurrence. The present two cases demonstrated that gliomatosis cerebri, classified among brain tumors of unknown origin by the world health organization, may transform into highly proliferative circumscribed tumors, in spite of their good response to radiotherapy. Examination of pathological features and their correlation with MRI findings may allow us to better understand the response to radiotherapy and the process of recurrence. ( info)

10/754. Malignant glial tumor arising from the site of a previous hamartoma/ganglioglioma: coincidence or malignant transformation?

    Gangliogliomas are generally considered benign tumors. Although more commonly found in the brain, spinal cord ganglioglioma is a well established, albeit infrequent, entity. We describe a 2-decade clinical course of a patient initially diagnosed with a thoracolumbar 'glial-neuronal hamartoma' at age 4. Seventeen years after his first operation, local recurrence was noted. Despite subsequent multiple gross total resections and adjuvant therapy, histologic features became increasingly ominous and ultimately proved fatal. This is an unusual report and histologic presentation of a resected spinal cord ganglioglioma recurring as an anaplastic ependymoma/astrocytoma and subsequently a glioblastoma. It is quite likely that the originally resected ganglioglioma was actually part of a primitive neuroectodermal tumor which had undergone extensive maturation. ( info)
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